Peripheral Vascular Disease Flashcards
There are how many types of blood vessels?
5
What are the types of blood vessels?
Veins
Venules
Capillaries
Arteries
Arterioles
Blood vessels that carry deoxygenated blood, Thin, less muscular wall
Veins/ venules
Blood vessel with 3 less defined layers
Veins/ venules
Blood vessels that distend more than arteries
Veins/ venules
Blood vessels with valves to prevent backward flow
Veins/ venules
75% total blood volume is in the
veins
SNS can stimulate constriction of these blood vessels
veins
These blood vessels use contraction of skeletal muscles to move blood flow
Veins/ venules
Single layer blood vessels with thin walls that permits transport
Capillaries
Blood vessels where oxygen and CO2 exchange
Capillaries
Blood vessels that carry oxygen rich blood
Arteries/Arterioles
Blood vessels with thick walls and three distinct layers
Arteries/Arterioles
The inner layers of the arteries/ arterioles are
smooth
The middle layer of the arteries/ arterioles
dilates/constricts
The outer layer of the arteries/ arterioles
Anchor vessels
Blood vessels where chemical, hormonal, neuronal factors effect constriction and dilation
Arteries/Arterioles
The lymphatic system collects lymph from tissues and organs and transports into
venous circulation
Permeable to large molecules ie: protein
lymph
Muscular contraction of walls and tissue propels lymph towards
venous drainage
Excess fluid from the arterial-venous filtration is absorbed by
lymphatic circulation
Runs alongside the capillary bed
lymphatic system
Hardening of arteries
Arteriosclerosis
Plaque formation
Atherosclerosis
Injury to endothelium causes platelets and monocytes
to aggregate
Two types of lesions
Fatty streaks
fibrous plaques
Decreased flow of oxygen rich blood due to narrowed arterial lumen is caused by
Arteriosclerosis and atherosclerosis
Increased metabolic demands caused by arteriosclerosis and atherosclerosis leads to
ischemia
ischemia
an inadequate blood supply to an organ or part of the body causing pain
Smoking increases platelet aggregation leading to
clot formation
aggregation
clustering
Atherosclerosis clinical manifestations:
Coronary arteries
angina, MI
Atherosclerosis clinical manifestations:
Cerebral arteries
Stroke , TIA’s
Atherosclerosis clinical manifestations:
Aorta
aneurysm
Atherosclerosis of Extremities
Peripheral Artery Disease
Number 1 sign of Peripheral Artery Disease
Intermittent claudication
Pain caused by too little blood flow to muscles during exercise.
Claudication
What do the legs/feet look like with PAD?
Thin brittle shiny skin on legs/feet
Loss of hair on legs
Dependent rubor
Thickened toenails
What might you find while assessing legs/feet with PAD?
Diminished peripheral pulses
Prolonged capillary refill
Patients with advanced PAD will feel
Pain at rest
Patients with PAD may have what kind of ulcers?
dry, necrotic, delayed healing
Pain is distal to
diseased artery
Claudication may begin shortly after
activity begins
PAD:
Elevating legs makes pain _____ and foot becomes _____
worse and foot becomes pale
PAD:
Dangling (dependent) legs does what to pain? What color do the feet turn?
relieves pain – foot becomes deep red (rubor)
PAD:
Med that improves blood flow
Cilostazol
Onychomycosis is
A fungal infection of the nail
PAD diagnostic tests:
Sees blood flow in legs
Doppler study
PAD diagnostic tests:
Testing for claudication
Treadmill test
PAD diagnostic tests:
combines both ultrasound and Doppler procedures. The result is live, high-definition pictures of blood flow.
Duplex ultrasound
PAD diagnostic tests:
Non-invasive test performed by measuring the systolic blood pressure from both brachial arteries and from both the dorsalis pedis and posterior tibial arteries after the patient has been at rest in the supine position for 10 minutes
Arterial Brachial Index (ABI)
What patients need ABI?
Pt with diminished pulses
50 y or older with history of diabetes
Patients with an ABI <0.9 =
PAD
NORMAL ABI is
1 – 1.4
NORMAL ABI is because feet arterial BP
Is slightly higher than brachial
Cilostazol should enable pt to
walk longer periods of time without pain
Pt will aortoiliac disease –
assess femoral pulse
Carbon monoxide from tobacco binds to
hemoglobin depriving tissues of oxygen
Fluid exchange across capillary wall based on
hydrostatic and osmotic forces.
Hydrostatic pressure at arterial end is higher then
venous
Hydrostatic pressure at arterial end drives fluid into the
tissue space
At venous end of capillary, osmotic forces
reabsorb fluid back into capillary.
Any left over fluid goes into
lymphatic vessels
Interpretation of ABI:
> 1.30
Noncompressible
Interpretation of ABI:
0.41 - 0.90
Mid-Moderate PAD
Interpretation of ABI:
0.00 - 0.40
Severe PAD
PAD patient teaching
Promote exercise, dangle legs, do not elevated, no crossing legs, no heating pads
Weight reduction, smoking cessation, reduce BP
Platelet Inhibitors prevent
clots
Platelet Inhibitor med names
Aspirin
Clopidogrel (Plavix)
Cilostazol (Pletal)
Statins draw
cholesterol out of plaques
Endovascular Treatments
Balloon angioplasty, stent, atherectomy
After graft/stent, patient will likely be placed on
platelet inhibitor to keep stent/graft open
Surgery for partial and complete blockage
Bypass grafts
Autologous bypass graft
pt’s own vein
Dacron graft
Synthetic bypass graft
Nursing care post bypass
VS & Pulse check q15 min initially
Incision site – monitor for hematoma
Neurovascular checks (cap refill/temperature/color)
Edema expected, elevate EXT while in bed and ambulate as soon as possible
No leg crossing or prolonged dependent position
After fem-pop bypass – which pulse do you assess?
After fem-pop bypass, assess dorsalis pedis or tibial
Checking for complications:
Graft Occlusion
pallor, decreased pulses, cool skin temperature
Checking for complications:
Compartment Syndrome
Numbness, severe pain, edema, taunt skin
If there are complications after treatment surgery
Ambulate ASAP
Med given in recovery room
Plavix or may be kept on heparin drip
Stenosis and occlusions less frequent in
arms
Upper extremity arterial disease is usually the result of
atherosclerosis or trauma
S&S of Upper extremity arterial disease
Arm fatigue, pain with exercise, inability to hold objects
Cool, pales, decreased capillary refill
Diagnostic test to determine upper extremity arterial disease
Doppler studies
Artery providing blood flow to brain reverses to arm causing lightheadedness
Subclavian steal syndrome
Treatment for upper extremity arterial disease
PTA with stent or graft
PTA
Percutaneous Transluminal Angioplasty
Nursing after surgery for upper extremity arterial disease
Vascular checks – if no pulse – immediately contact physician
Keep arm at heart level or elevated after surgery
Aching/burning is ischemia, but a complete occlusion is
more severe pain, or complete loss of sensation
6 P’s
Pain
Pallor
Pulselessness
Paresthesia
Poikilothermia
Paralysis
Poikilothermia
the inability to regulate core body temperature
Parasthesia
Pins and needles
COLD / PALE FOOT – will turn
dusky
Balloon tipped catheter that removes embolus
Emergency embolectomy
If patient has adequate collateral circulation
Heparin or t-PA is given
t-PA :
tissue plasminogen activator (clot buster), an injection given right into clot
Arterial occlusions are diagnosed with
ultrasound and arteriogram
Nursing Management of arterial occlusion:
Prior to intervention:
BEDREST
Affected EXT level or slightly dependent
Keep EXT room temperature (no heating/cooling pads)
Nursing Management of arterial occlusion:
Med stopped 30 minutes prior to surgery
IV Heparin
Intermittent arteriolar vasoconstriction
Results in coldness/pallor/pain of fingertips, toes
Raynaud’s phenomenon
Reynaud’s:
Rebound circulation causes
redness and pain
Skin color changes associated with Raynaud’s
WHITE – then BLUE because of pooling of deoxygenated blood the RED from exaggerated blood flow during vasodilation
Raynaud’s phenomenon stimulus:
Cold, Stress, Nicotine
Raynaud’s phenomenon Treatment:
usually none required, possible Calcium Channel Blocker
idiopathic
no other condition (genetic)
Veins that lie just under the skin
Superficial Veins
Veins that run parallel to arteries
Deep Veins
Venous disorders cause
reduction in venous blood flow back up to heart
Result of Venous disorders
stasis of blood, edema, tissue breakdown (ulcers/cellulitis), increased susceptibility to cellulitis
Small vessels rupture from pressure, rbc’s escape into surrounding tissue
Hemosiderin
Chronic distension from increased pressure and incompetent valves
Chronic Venous insufficiency
Risk factors for Chronic Venous insufficiency:
Obesity, immobility, pregnancy, history of DVT
S&S of Chronic venous insufficiency:
edema, discolored skin – hemosiderin, draining wounds
Treatment for Chronic Venous insufficiency:
Elevate legs
Compression stockings
Monitor for complications (cellulitis/wounds)
S&S of Venous insufficiency
Varicose veins
Darkened, hard, leathery skin
Pain and heaviness
Restless leg syndrome
leg cramps or spasms (NOT intermittent claudication)
Itchy skin
Yellow toenails
Virchow Triad
1) Hypercoagulability
2) Stasis
3) Vascular injury
VTE
Venous thromboembolism
Hypercoagulability state
Clotting too much
Most common cause of this VTE factor:
Cancer malignancy
pregnancy and peri-partum (because of hormones)
Oestrogen therapy
Trauma or surgery of lower half of body
Hypercoagulability state
Venous wall gets nicked or damaged
Vascular wall injury
Most common cause of this VTE factor:
Trauma/injury
Venipuncture
Chemical irritation
Heart valve disease or replacement
Atherosclerosis
Indwelling catheters
Vascular wall injury
When blood is not moving
Circulatory stasis
Most common cause of this VTE factor:
Atrial fibrillation
Left ventricular dysfunction
Venous insufficiency or varicose veins
Venous obstruction from tumor
Obesity or pregnancy
Bedrest
Post op
Circulatory stasis
Aggregates of platelets within the vein, attached to wall
More common in lower EXT’s
Deep vein thrombosis
The 3 causes of deep vein thrombosis:
vein injury (phlebitis from IV/chemo),
stasis
hypercoagulability
Clinical Manifestations of deep vein thrombosis:
Unilateral swelling of effected leg
Deep vein: edema, swelling, warmth, tenderness, red, concern of PE
Superficial veins: similar, usually dissolve spontaneously
Homan’s sign
Treatments for deep vein thrombosis
Anticoagulant therapy (monitor labs to direct)
elevate legs - pillow under legs not knee
compression stocking
Thrombectomy – mechanical clot removal with balloon stent
Once anticoagulation therapy started –
ambulate as soon as possible
Diagnosing DVT
Blood work (coagulation studies),D dimer, duplex ultrasound
Obstruction of pulmonary artery or one of its branches by a thrombus that originated in VENOUS system OR right side of heart
Pulmonary embolism (PE)
Symptoms of PE depend on
size of thrombus and area of pulmonary artery occluded
Symptoms of PE:
DYSPNEA
Chest pain, anxiety, tachycardia, dry cough
Diagnosing PE :
CT Angiogram or V/Q SCAN
Medical management of a stable patient with PE:
Lovenox/heparin
Medical management of an unstable patient with PE:
Thrombolytic therapy
Embolectomy – Interventional radiology
PE is not a ventilation problem, it is a
Perfusion problem
Most dangerous form of PE
Saddle PE
Nursing care of patient with PE
Monitoring thrombolytic therapy
Bleeding precautions
Manage Pain
Manage oxygen therapy
Relieve anxiety
Education : Patient will be discharged on long term anticoagulation
IVC filter placement (in groin) before discharge
IVC (inferior vena cava) filter does what? For how long?
Catches clots. Left in for one year
Platelet inhibitors & Anticoagulants does what to clots?
slow, stop, prevent clot. DOES NOT BREAK
Names of platelet inhibitors :
acetylsalicylic acid (Aspirin)
clopidogrel (Plavix)
cilostazol (Pletal)
Anticoagulant PO med that blocks liver’s use of vit K to produce clotting factors. Takes up to 72 hours to work
No precise antidote, but can give VIT K
Warfarin (Coumadin)
Newer PO anticoagulant meds:
no specific blood tests to monitor
No specific antidote exists
Can not stop taking suddenly
Dabigatran (Pradaxa)
Rivaroxaban (Xarelto)
Apixaban (ELIQUIS) PO only
INR
International Normalized Ratio
Foods that should be reduced/ eaten in moderation while taking warfarin (coumadin)
Green, leafy vegs
Give more coumadin when INR is
below 2
Give less coumadin when INR is
above 3
Normal INR is
between 2-3
Injectable anticoagulants that act rapidly to block formation of thrombin from prothrombin
Enoxaparin (Lovenox) (SQ)
Heparin (IV or SQ prophylactic)
Rate of heparin determined protocol –
aPTT lab values should be higher that normal with heparin(1.5 – 2.5 times normal Aptt = 60-80)
Will continue use of Heparin while starting Warfarin until
INR is 2
Antidote to Heparin :
protamine sulfate
Lovenox can be used for DVT, post operative, what type of surgery?
ortho surgery
All patients on heparin:
Bleeding precautions
all stool is tested for blood (guaiac)
CBC is usually daily – not every 3 days
HIT
Heparin induced thrombocytopenia
Low platelet count due to heparin
HIT - Heparin induced thrombocytopenia
Abnormally dilated, tortuous veins
Incompetent valves
Varicose veins
Clinical Manifestations of varicose veins:
Asymptomatic if superficial
Deep veins – dull ache, cramps heaviness, fatigue, swelling
Nonsurgical treatments for varicose veins:
Thermal Ablation, sclerotherapy, laser
Surgical treatments for varicose veins:
Ligation and stripping – vein is pulled out with the metal wire
Compression therapy is mostly done with what type of ulcer?
venous ulcers
Mechanical debridement –
wet-to-dry dressings
Autolytic debridement –
application of dressings that allow lysozymes in wound exudate to naturally breakdown nonviable tissue – Aquacel
Autolytic debridement med
Aquacel
Aquacel holds a lot of
drainage
Chemical debridement med
Santyl (collagenase)
Ulcer treatments
Antiseptic agents
Antibiotics
Debridement
hyperbaric oxygenation
wound vac
What kind of diet is appropriate for a patient with leg ulcers?
High protein diet rich in vitamins
Condition where the Microbes enter skin via entry point,
Toxins released into subcutaneous tissues, causing Swelling, redness, warmth and pain
Cellulitis